>> However, I also cited a paper at the recent Society for Neuroscience
> meeting relating mast cell proliferation in the thalamus, preceding
> focal lesions in thiamine-deficient rats. I read this as an argument
> for a gradual process, but it occurs to me now that although perhaps
> contributing to prodromal symptoms they could be activated in the rapid
> lesioning processes precipitated by a sudden demannd (e.g. glucose
> infusion). What is your thinking on this?
>The mast cell is a histamine-containing element of the immune system, and I
could only hazard a guess as to why mast cells should accumulate in the
thalamus during advanced thiamin deficiency in rats.
There is a direct correlation between the thiamin content of a cell and its
level of metabilic activity. As I noted before, thiamin's membrane functions
are intimately connected to solute transport reactions of a chemiosmotic
variety. Brain vascular tissues maintain a "blood-brain" barrier that acts to
keep out of neural networks many compounds that are otherwise present in blood
and delivered to organs other than the brain. Thiamin deficiency is known to
cause a breakdown in these barrier functions. This would allow molecules that
do not normally appear in brain tissues to diffuse into the extracellular
matrix. Perhaps in this location these molecules cause a mast cell mediated
form of "allergy". It is just a guess.
Robert D. Brown, MD
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